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Researcher's Profile

Toshiro FUJITA

Clinical Epigenetics


Tel: 03-5452-5070

FAX: 03-5452-5069

2019 Research book (PDF: 1.1MB)


1972. 03  Graduated from Keio University School of Medicine
1977. 01  Visiting Scientist, National Institutes of Health
1978. 07  Assistant Professor, Department of Internal Medicine, University of Tsukuba
1988. 04  Assistant Professor, Fourth Department of Internal Medicine, The University of Tokyo (UTokyo) School of Medicine
1989. 06  Associate Professor, Fourth Department of Internal Medicine, UTokyo School of Medicine
1995. 03  Professor, Fourth Department of Internal Medicine, UTokyo School of Medicine
1997. 04 Professor, Department of Nephrology and Endocrinology, Graduate School of Medicine, UTokyo
2012. 04 Project Professor, Division of Clinical Epigenetics, RCAST, UTokyo
2012. 06 Emeritus Professor, UTokyo
2018. 04 Distinguished Research Professor, Shinshu University
2018. 04 Fellow, RCAST, UTokyo

Research Interests

Our laboratory has continuously been trying to clarify the pathophysiology of lifestyle diseases and to discover effective countermeasures to restore health. Our recent project has centered around the mechanisms of hypertension and organ damage induced by excess salt. We have found that a small GTPase, Rac1, activates the mineralocorticoid receptor (MR) which regulates the internal sodium balance and blood pressure, independently from aldosterone. We have also shown that an aberrant Rac1-MR pathway is involved in the development of salt-induced hypertension. Moreover, an epigenetic mechanism plays an important role in the salt-induced hypertension evoked by sympathetic overactivity, through the suppression of WNK4, which increases the reabsorption of sodium in the renal tubules, and causes internal sodium retention resulting in hypertension. Currently, we are exploring how epigenetics is involved in the progression of kidney disease caused by diabetes and hypertension. We suspect that excess intake of salt or calories can modulate the regulation of gene transcription which leads to the onset of lifestyle diseases such diabetes or hypertension. Our goal is to systematically elucidate the mechanism for the epigenetic regulation of gene transcription in hypertension and diabetes. Moreover, epigenetics is known to be involved in the progression of organ damage, and our intriguing mission is to elucidate the mechanism and apply this knowledge to the development of new therapies.

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